Glutamate is the primary excitatory neurotransmitter in the mammalian brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Baum, Larry PhD; Lam, Christopher Wai Kei PhD; Cheung, Stanley Kwok-Kuen MSc; Kwok, Timothy MD; Lui, Victor MRCPsych; Tsoh, Joshua MRCPsych; Lam, Linda MD, MRCPsych; Leung, Vivian FHKCPsy; Hui, Elsie FRCP; Ng, Chelsia HBSc; Woo, Jean MD; Chiu, Helen Fung Kum FRCPsych; Goggins, William B. ScD; Zee, Benny Chung-Ying PhD; Cheng, King Fai MD; Fong, Carmen Yuet Shim RN; Wong, Adrian BSc; Mok, Hazel BSc; Chow, Moses Sing Sum PharmD; Ho, Ping Chuen PhD; Ip, Siu Po PhD; Ho, Chung Shun PhD; Yu, Xiong Wen PhD; Lai, Caroline Yau Lin MMedSc; Chan, Ming-Houng FHKCPhys; Szeto, Samuel FRCP; Chan, Iris Hiu Shuen PhD; Mok, Vincent MD Author Information 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Delivery of cognitive rehabilitation by telehealth appeared feasible but required modifications such as greater reliance on caregivers and clients for manipulating materials. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
High-dose vitamin supplementation reduces homocysteine levels in patients with AD. 2 key findings →
Design: open-label trial Participants: 69 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Donepezil and silymarin improved lipid profile associated with increased NAA/Cr, and decreased mI/Cr, in AD patients. 4 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The ASURE trial design is discussed, with a particular focus on fluid biomarkers, EEG, and CFC as endpoints. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is characterized by the accumulation of beta-amyloid (Aβ) plaques and neurofibrillary tangles composed of hyperphosphorylated tau, which together lead to neurodegeneration and cognitive decline. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The burden of Alzheimer disease (AD) on the US healthcare system is substantial and increasing. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
and neurogranin changes correlated with sabirnetug-AβO target engagement (p ≤ 0.01). 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In this study, 122 individuals were divided into two groups. 5 key findings →
Participants: 122 Evidence: low
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Cognitive training, whether combined with active or sham tDCS, led to significantly increased fractional anisotropy averaged across all brain regions, indicating an overall improvement in white matter integrity. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
A greater number of needs (B=.42), polypharmacy (B=.33), and unmanaged symptoms (B=.31) significantly predicted higher triage priority (p<.001). 1 key finding →
Participants: 461 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
39/100
Alzheimer's disease (AD)-a complex disease showing multiple pathomechanistic alterations-is triggered by nonlinear dynamic interactions of genetic/epigenetic and environmental risk factors, which, ultimately, converge into a biologically heterogeneous disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The recent failure of several clinical trials on anti-β-amyloid (Aβ) drugs in Alzheimer's disease (AD) suggested earlier intervention in the disease course. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease progressively impairs cognition and daily function, and death usually occurs five to ten years after diagnosis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Efforts to develop effective disease-modifying treatments for Alzheimer's disease (AD) have mostly targeted the amyloid β (Aβ) protein; however, there has recently been increased interest in other targets including phosphorylated tau and other forms of tau. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Progressive supranuclear palsy (PSP) is a common cause of atypical parkinsonism and a rapidly progressive disease that greatly burdens both patients and caregivers. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
In 2011, a hexanucleotide repeat expansion in the first intron of the C9orf72 gene was identified as the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
LMTM given alone increased hippocampal Acetylcholine (ACh) levels, glutamate release from synaptosomal preparations, synaptophysin levels in multiple brain regions and mitochondrial complex IV activity, reduced tau pathology, partially restored ChAT immunoreactivity in the basal forebrain and reversed deficits in spatial learning. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common cause of dementia in the elderly. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Phases 1 and 2 results facilitated targeted changes in BESI, thus improving its overall usability for the final phase of the study, when real-time notifications and interventions will be implemented. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
AimTo explore the experiences and challenges for residential care home staff when managing the healthcare needs of their residents, in particular those living with dementia. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with early symptomatic Alzheimer's disease showed less cognitive and functional decline with donanemab compared with placebo in a Phase 2 study offering up to 72 weeks of treatment. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical trial registration www. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There are many who feel that the achievement of a disease-modifying (DM) designation for a drug is an important goal in Alzheimer disease (AD) therapeutics. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Where “Free full text” comes from
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
How the 0–100 score works — and why some entries are capped
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 27,380 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,032 records (3.8% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →